We are analyzing https://link.springer.com/article/10.1007/s11010-024-05062-5.

Title:
Cell death crosstalk in respiratory diseases: unveiling the relationship between pyroptosis and ferroptosis in asthma and COPD | Molecular and Cellular Biochemistry
Description:
Asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous obstructive diseases characterized by airflow limitations and are recognized as significant contributors to fatality all over the globe. Asthma accounts for about 4, 55,000 deaths, and COPD is the 3rd leading contributor of mortality worldwide. The pathogenesis of these two obstructive disorders is complex and involves numerous mechanistic pathways, including inflammation-mediated and non-inflammation-mediated pathways. Among all the pathological categorizations, programmed cell deaths (PCDs) play a dominating role in the progression of these obstructive diseases. The two major PCDs that are involved in structural and functional remodeling in the progression of asthma and COPD are Pyroptosis and Ferroptosis. Pyroptosis is a PCD mechanism mediated by the activation of the Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome, leading to the maturation and release of Interleukin-1β and Interleukin-18, whereas ferroptosis is a lipid peroxidation-associated cell death. In this review, the major molecular pathways contributing to these multifaceted cell deaths have been discussed, and crosstalk among them regarding the pathogenesis of asthma and COPD has been highlighted. Further, the possible therapeutic approaches that can be utilized to mitigate both cell deaths at once have also been illustrated.
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Keywords {🔍}

pubmed, article, google, scholar, cas, central, cell, ferroptosis, wang, zhang, pyroptosis, chen, asthma, liu, inflammasome, httpsdoiorgs, death, disease, inflammation, nlrp, copd, obstructive, med, cancer, airway, sci, yang, chronic, activation, lung, mol, pulmonary, immunol, cells, role, biol, res, zhao, pathway, epithelial, int, jiang, signaling, nat, zhu, sun, zhou, nature, caspase, pathways,

Topics {✒️}

int/news-room/fact-sheets/detail/chronicobstructive-pulmonary-disease tlr4-nf-κb-myd88 signalling pathway tlr4/myd88/nf-κb pathway tlr4/nf-κb signaling pathway tlr4/nf-kb signaling pathway ros-mediated nf-κb suppression month download article/chapter suppressing tlr-4/nf-κb pathway tlr4/myd88/nf-κb il-13-challenged beas-2b cells cigarette smoke-induced activation modifies lipopolysaccharide-mediated responses sepsis-induced lung injury fatty acid β-oxidation toluene diisocyanate-induced asthma inflammation-related respiratory disease nlrp3-dependent il-1 production ptgs2/pge2 signaling pathway induce il-1β secretion ova-induced asthma model activating nrf2-mediated pathway nrf2/ho-1 signaling pathways p53-independent tumor suppression pd-l1-mediated gasdermin ros/nlrp3/caspase-1 pathway aim2 inflammasome-mediated pyroptosis increased il-1β levels resibufogenin suppresses growth short-term mouse model airway smooth muscle cigarette smoke induces birla institute article khawas neelima sharma designed damaged blood-brain barrier full article pdf shigella-induced apoptosis inflammatory signaling pathways acute lung injury inhibiting nf-κb nrf2 signaling pathway activates inflammasome-ferroptosis processes suppressing caspase-4/5/11/gsdmd-mediated attenuates airway inflammation lipid death signals inducing caspase-1-dependent pyroptosis ten hacken nh vanaja sk potential targeted therapies lung epithelial injury

Questions {❓}

Xia X, Wang X, Cheng Z, Qin W, Lei L, Jiang J, Hu J (2019) The role of pyroptosis in cancer: pro-cancer or pro-“host”?

Schema {🗺️}

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      description:Asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous obstructive diseases characterized by airflow limitations and are recognized as significant contributors to fatality all over the globe. Asthma accounts for about 4, 55,000 deaths, and COPD is the 3rd leading contributor of mortality worldwide. The pathogenesis of these two obstructive disorders is complex and involves numerous mechanistic pathways, including inflammation-mediated and non-inflammation-mediated pathways. Among all the pathological categorizations, programmed cell deaths (PCDs) play a dominating role in the progression of these obstructive diseases. The two major PCDs that are involved in structural and functional remodeling in the progression of asthma and COPD are Pyroptosis and Ferroptosis. Pyroptosis is a PCD mechanism mediated by the activation of the Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome, leading to the maturation and release of Interleukin-1β and Interleukin-18, whereas ferroptosis is a lipid peroxidation-associated cell death. In this review, the major molecular pathways contributing to these multifaceted cell deaths have been discussed, and crosstalk among them regarding the pathogenesis of asthma and COPD has been highlighted. Further, the possible therapeutic approaches that can be utilized to mitigate both cell deaths at once have also been illustrated.
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         Medical Biochemistry
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